Aminoglycoside nephrotoxicity will be investigated in terms of both the transport of aminoglycosides into kidney cells and the ultimate biochemical site of toxicity. Parallel studies will be carried out to define more fully the mechanism of transport of aminoglycosides into bacterial cells. Chloramphenicol toxicity (including the gray baby syndrome, transient bone marrow suppression, and aplastic anemia) will be investigated, in terms of the contributions of defective or supernormal glucuronidization to the toxicity or ineffectiveness respectively of the drug. More information will also be sought on the biochemical events that might underly these toxicities. The pharmacologic modulation of immune responses may be placed on more rational grounds by understanding more of the individual reactions of the immune responses. The potential role of alpha 1-antitrypsin, a serine protease inhibitor, in the process of mitogenesis has been demonstrated and this phenomenon will be explored in greater depth. The effects of chloramphenicol, other antibiotics, and other drugs will be investigated with respect to effects on cell division and cell migration as two important parts of an immune response.